15 Things No One Tells You About Alzheimer’s Disease

Every 65 seconds, someone develops Alzheimer’s, and their family and friends must become caregivers. Experts share the 15 things no one tells you about the challenges—and rewards.

Your loved one may do wildly inappropriate things

Senior woman with walking stick being helped by a female nurse at home. Full length shot of female doctor with elderly patient at nursing home.JACOB LUND/SHUTTERSTOCK

“Sometimes people say and do things that are out of character,” says Ruth Drew, director of Information and Support at Alzheimer’s Association. She recalls the time a woman—who had always been very proper—began taking off her clothes from the waist down. One of the residential care facilitators suspected that there was something going on and had her tested for a urinary tract infection—which turned out to be the problem. “You need to play detective and discover what is triggering the behavior,” says Drew.  “The circle of life reverses itself and sometimes the child becomes the parent,” notes Gail Pearson, Memory Care Unit Manager, Jeffrey and Susan Brudnick Center for Living.

Loss of inhibitions

Pleasant memories. Portrait of old charming couple remembering sweet moments. Woman is looking at husband while laughing. Man is regarding at picture while tenderly cuddling wifeOLENA YAKOBCHUK/SHUTTERSTOCK

“It is not uncommon that my husband opens his zipper. He doesn’t do it to be sexual. He thinks it’s funny,” reports a family caregiver. “He also tries to kiss strangers because he truly believes everyone likes him.”

Expect delusions and hallucinations

15 Things No One Tells You About Alzheimer's DiseaseLOGOBOOM/SHUTTERSTOCK

“Delusions can turn on a dime,” notes Pearson. Patients may say sexually inappropriate comments because they have no filter, she says.

Speech may disappear

Thoughtful retiree looking what going onOLENA YAKOBCHUK/SHUTTERSTOCK

Even though she had been a social worker for over two decades, Tanjulla Tyson-Wearren was surprised when her mother suddenly couldn’t speak. “It was an emotional roller coaster. I was not prepared to never hear her sing a song or say hi,” says Tyson-Wearren. “Even when they cannot speak, there are still ways to connect, “says Drew.

They may forget how to shower


“Confusion becomes the central way of thinking,” notes Crystal Polizzotti, Healthy Aging Program Manager at Elder Services of the Merrimack Valley. Polizzotti notes that there are about 15 steps to taking a shower that we don’t even think about—but that a person with Alzheimer’s may find impossible to complete. One of the caregivers told Polizzotti that the only way she could get her husband to shower was to go in first. “You have to get creative,” notes Polizzotti.

Alzheimer’s is deadly


It’s the sixth leading cause of death, Drew points out: “A lot of people still do not understand that Alzheimer’s cannot be prevented, slowed down, or cured.” The Alzheimer’s Association’s Annual Report notes that one in three seniors will die with Alzheimer’s or another form of dementia. Alzheimer’s kills more people than breast cancer and prostate cancer combined.

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Bipolar Disorder Increases Parkinson’s Risk Sevenfold

Bipolar patients are seven times more likely to develop Parkinson’s disease, according to a new study. Though the news may be disheartening to those suffering from the already-trying condition, the link might also lead to clues about the causes behind the two conditions.

Parkinson’s is a complex disease associated with a gradual decline in dopamine levels produced by neurons, or brain cells. It eventually leads to impaired movements and other bodily functions. The causes are unknown, and there is no cure.

Bipolar disorder, also known as manic-depressive illness, is characterized by episodic fluctuations in mood, concentration or energy levels. Its causes are also unknown, though some bipolar-associated genes have been identified. Researchers are still figuring out how brain structure and function changes under the disease.

Previous research has linked Parkinson’s with depression. So when the authors of the new study, most of whom are practicing physicians, noticed some of their bipolar patients developing Parkinson’s, they wondered if there was a connection.

Seven Times The Risk

The study, out today in Neurology, was led by Huang Mao-Hsuan, who practices in the department of psychiatry at Taipei Veterans General Hospital. The researchers compared data from two groups of adults in the Taiwan National Health Insurance Research Database. Members of one group — over 56,000 individuals — were diagnosed with bipolar disorder between 2001 and 2009. The other — 225,000 individuals — had never been diagnosed with the disorder. No one in either cohort had received a Parkinson’s diagnosis and all the patients were over 20. And researchers ensured the two groups had similar ages, socioeconomic status, and other traits that might influence health.

You Might Like: Child Bipolar Disorder Still Rare

The researchers followed up with all 278,000 people in 2011 to see how many had been subsequently diagnosed with Parkinson’s. They found that 0.7 percent of the patients with bipolar disorder ended up developing the disease — about 1 in 140. But for those without the disorder, the prevalence of Parkinson’s was about 1 in 1,000, or 0.1 percent.

Link Uncertain

Researchers found the trend held even when controlling for the potential effects of antipsychotic medications, which are frequently prescribed for bipolar disorder and are known to cause Parkinson’s-like symptoms (known as drug-induced parkinsonism, or DIP.)

The only clue to a mechanism that would explain the link was that patients with the highest frequency of psychiatric admission for bipolar episodes also had the highest prevalence of Parkinson’s. It’s not clear why this would be, though both bipolar disorder and Parkinson’s are known to be linked to impaired dopamine transmission in the brain. More research is needed to figure out what the connection between these two diseases might be.

You Might Like: Bipolar Disorder – A BRIDGE to nowhere?

Child Bipolar Disorder Still Rare

Bipolar disorder usually strikes between the ages of 15 and 25, and is extremely rare in preteens, according to a major study: Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patients

The findings are old hat. It’s long been known that manic-depression most often begins around the age of 20, give or take a few years. Onset in later life is less common while earlier onset is very unusual.

The main graph could have been lifted from any psychiatry textbooks of the last century:

The red bars are the data. Ignore the black line, that just shows an imaginary ‘even’ distribution over the lifespan.

Why am I blogging about these remarkably unremarkable results? Because they undermines the theory, popular in certain quarters but highly controversial, that ‘child bipolar’ or ‘pediatric bipolar’ is a major health problem.

The study confirmed that early-onset bipolar I does exist, but just 5% of the bipolar I patients had an onset before the age of 15. Assuming a lifetime prevalence of 1% for bipolar I disorder, which is about right, that makes about 0.05%, 1 in 2000 kids, about the same prevalence as Down’s Syndrome. Even that’s an overestimate, though, because this sample was enriched for early-onset cases: some of the participating clinics were child and adolescent only.

There’s a few caveats. This was a retrospective study, that took adults diagnosed bipolar, and asked when their symptoms first appeared. It’s possible that early onset cases were under-sampled, if they were less likely to survive to adulthood, or get treated. The generally milder bipolar II might also be different from the bipolar I studied here. But in general, these numbers support the traditional view that childhood bipolar is just not very prevalent.

Bipolar Disorder – A BRIDGE to nowhere?

Last August I blogged about a research paper that claimed that almost half of all people suffering from depression actually have features of bipolar disorder – including me: So Apparantly I’m Bipolar

It was called the BRIDGE study. I took issue with it for various reasons, including the fact that it counted as ‘bipolar features’ any periods of irritable or elevated mood, even if they were associated with drug treatment:

Under the new regime if you’ve ever been irritable, high, agitated or hyperactive, on antidepressants or not, you meet “Bipolar Specifier” criteria, so long as it was marked enough that someone else noticed it…

A cynic would say that this is a breathtaking piece of psychiatric marketing. You give people antidepressants, then you diagnose them with bipolar on the basis of their reaction to those drugs, thus justifying selling them yet more drugs.

The cynic would not be surprised to learn that this study was sponsored by pharmaceutical company Sanofi.

Now a crack team of psychiatrists have written a Letter to the Editor criticizing BRIDGE and they say… pretty much what I said: BRIDGE Study Warrants Critique. They do make a couple of new points also.

The 8 authors of the Letter include David Allen, David Healy, Peter Parry and Jon Jureidini, all major critical voices in psychiatry. However… while this A-Team make an excellent case that BRIDGE is a step in the direction of overdiagnosis and overtreatment of bipolar, they drop the ball slightly when they say:

The article concluded with an appeal to use “mood stabilizers,” presumably atypical antipsychotics, which are less efficacious than lithium. The sponsor has a medication in this class.

Sanofi does make the atypical antipsychotic amisulpiride, but it’s not generally referred to as a “mood stabilizer”, and I’m not sure why you’d assume that Sanofi had amisulpiride specifically in mind. The BRIDGE team exploit this in their rebuttal letter:

Allen et al cast unseemly aspersions that the BRIDGE study was a vehicle to promote sales of an antipsychotic drug sold by sanofi-aventis. sanofi-aventis has no antipsychotic with an indication for bipolar disorder. We know of no evidence that this was the case at any stage of development and execution of the BRIDGE study.

Maybe so, but as I said in my post, Sanofi also make some popular brands of valproate/valproic acid, a prototypical “mood stabilizer” which is widely used in bipolar disorder. I’d have said that was the more likely candidate…

Fundamentally, we know that Sanofi “was involved in the study design, conduct, monitoring, data analysis, and preparation of the report.” We also know that Sanofi is exists to make profit by selling drugs. So either Sanofi thought that this study would make them a profit eventually, by selling more drugs… or they threw money and time at this for no commercial reason. Hmm.

The reply concludes with the frankly bizarre statement that:

Allen et al view their position as part of a “debate” about the “ever-widening bipolar spectrum.” We consider data, not debates, as central to the progress in the scientific understanding of mood disorders…

But science is a debate about data. Data by themselves are just numbers; to be useful, they must be interpreted, and scientific debates aim at arriving at such interpretations. No-one is questioning the BRIDGE data as such, we’re questioning what it means.

Lyme Disease 10 Times More Prevalent Than Previously Thought

The CDC now estimates that 300,000 Americans are infected with Lyme — and other tick-borne illnesses are a growing threat as well.

Control and Prevention (CDC) estimated last summer that the number of people diagnosed with Lyme disease each year was 300,000 — 10 times as high as the official counts — the agency must have expected headlines, and it got them. The alarmingly high figure justified assertions by patient advocacy groups that the 30,000 cases reported annually were just the tip of the iceberg.

The erythema migrans rash is a classic, though not universal, sign of Lyme disease.
James Gathany/CDC

Lyme disease is caused by a bacterium, Borrelia burgdorferi, which is transmitted by black-legged ticks. Infection results in fever, headache, fatigue and, in many cases, a distinctive oval rash called an erythema migrans. Untreated, Lyme may advance to painful complications of the joints and nervous system. The disease is concentrated in the Northeast and upper Midwest, and in parts of the Pacific Northwest. The CDC is notified of cases by doctors, laboratories and local health departments.

Despite the new numbers, epidemiologist Paul Mead, in charge of the agency’s Lyme program, challenges the idea that there’s been a “whopping surge” in Lyme disease. The CDC has long known that “the physician may not fill out the form, or the lab doesn’t submit its form properly,” says Mead. But only now do researchers have the evidence to back up the claim.

Black-legged ticks transmit Borrelia burgdorferi, the bacterium that causes Lyme disease.
Robin Treadwell/Science Source

To get more accurate numbers, the CDC team conducted three overlapping surveys. In one, they examined medical insurance claims for 22 million people over six years. In the second, they checked the records of seven major commercial labs that run blood tests for Lyme. And in the third, they polled representative Americans by telephone, asking if they’d been diagnosed.

If the actual number of new cases each year is around 300,000, it’s “a tremendous public health problem,” says Mead. Although the incidence did not jump tenfold overnight, the problem has grown steadily worse in the 30 years since the disease was identified. “Tick-borne illnesses are on the rise,” says Mead, “and we’re having a hard time figuring out what to do about them.”

Lyme Disease’s Newfound Cousin

In January, tick-borne disease expert Peter Krause of Yale University and colleagues reported a new Lyme-like disease in the United States. After discovering the first human cases in Russia in 2011, Krause now thinks the disease — still too new to be named — could exist wherever hard-bodied ticks transmit Lyme.

The bacterial culprit, Borrelia miyamotoi, enters a person’s bloodstream via tick bite and elicits flulike symptoms similar to Lyme disease, but with a relapsing fever instead of the telltale bulls-eye rash. The fever develops as a person’s immune system designs and cranks out an antibody specific to the bacteria. But B. miyamotoi keeps changing outer-surface proteins, and the fever returns each time the immune system has to scramble to make a new antibody.

Although B. miyamotoi is less common than Lyme, it could turn out to be more insidious in one sense: While the Lyme bacteria die along with its host tick, B. miyamotoi is transmitted from a female tick to her eggs. Thus, the relapsing fever can be spread not only by adult and nymphal (adolescent) ticks, but also by the bite of newborn larvae.

Reporting in the New England Journal of Medicine, Krause says the cyclic and nonspecific symptoms of B. miyamotoi are problematic for doctors trying to identify the disease and for patients seeking treatment. But he expects diagnostic tests now in development will be widely available in a matter of months.  — Breanna Draxler

Scourge of Powassan

In August, a teenager in the Hudson Valley region of New York died from tick-borne Powassan virus, according to preliminary findings. The precise cause of death was encephalitis, an inflammation of the brain.

In research published just a month earlier, Richard Ostfeld of the Cary Institute of Ecosystem Studies and colleagues reported that the Powassan virus inhabits up to 6 percent of black-legged ticks in the region.

In terms of cases, “Powassan is dwarfed by Lyme disease,” says Ostfeld, “but the severity is so much greater. Your risk of dying is at least 10 percent. Your risk of being permanently disabled is 50 percent. And the tick can transmit the virus in 15 minutes. The good news is that it’s extremely rare.” — Jeff Wheelwright

Two independent mechanisms are involved in tuberous sclerosis

The current idea about how tuberous sclerosis occurs places mTORC1, a protein complex that regulates cell metabolism, as the major driving force behind the disease. But according to a new study published in the Proceedings of the National Academy of Sciences by researchers at Baylor College of Medicine and Texas Children’s Hospital, the development of this rare condition also involves a second mechanism that is independent of mTORC1. The findings can potentially lead to new treatments that might benefit patients who partially respond to current therapies focused on mTORC1.

“Tuberous sclerosis is a rare genetic disease that causes benign tumors to grow in the brain, kidneys, skin and other organs. Patients present with a combination of symptoms that can include seizures, developmental delay, skin abnormalities and kidney disease,” said first and co-corresponding author Dr. Rituraj Pal, postdoctoral associate of molecular and human genetics at Baylor.

Tuberous sclerosis is caused by mutations in the genes TSC1 and TSC2. The current thought is that the dysfunctional proteins produced by these mutated genes fail to regulate mTORC1, which then becomes hyperactive and leads to the development of the disease. How the disease actually develops is still not clear.

“Previous studies have associated tuberous sclerosis with excessive accumulation of glycogen, a main source of energy, inside cells, although this has not been clearly shown,” said corresponding author Dr. Marco Sardiello, assistant professor of molecular and human genetics at Baylor and a member of the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. “We know from other conditions that glycogen accumulation damages cells.”

Cells are like homes. Both are constantly producing waste that must be disposed of to keep a healthy, functional environment. Even materials that are usually not toxic, such as glycogen, will become so if they accumulate inside the cell. To gain insights into how the disease happens, the researchers first investigated whether glycogen accumulated inside cells with the disease.

Discovering a second player in tuberous sclerosis

“We clearly show that glycogen accumulates inside both human and mouse cells with the condition,” Pal said. “Then we investigated the mechanism.”

The researchers looked at mTORC1, the only player that was known to be contributing to tuberous sclerosis, and found that in some cases in which the TSC2 gene is completely deleted, mTORC1 is hyperactive and partially responsible for the accumulation of glycogen.

But when the researchers tested samples from patients carrying two particular TSC2 mutations that do not completely eliminate the gene but just change the protein, they observed that mTORC1 was working normally, yet glycogen accumulated inside the cells. This suggested that there was another glycogen-clearing mechanism at play and that it was independent of mTORC1.

“One clue about what the second mechanism might involve was the observation that the affected cells had fewer lysosomes than normal cells,” Pal said. “Lysosomes are structures in charge of clearing cellular waste. When lysosomes fail and cellular waste accumulates, disease follows.”

Further investigations showed that the second mTORC1-independent mechanism involved defects in the formation of lysosomes and in the process that digests cellular materials, including glycogen. And this led to the accumulation of glycogeninside the cells.

“Our findings put forward a new perspective on this disease that can have implications for patient treatment. We show that mutations of TSC2 are not all equal, implying that the same is true for patients,” Pal said.

Current treatments are focused on modifying only mTORC1 activity. This work suggests that further studies are needed to systematically analyze the TSC mutations carried by each patient. Some patients may be carrying TSC mutations that affect mTORC1. But in other patients TSC mutations may be affecting the second mechanism without disrupting mTORC1.

“This could lead to the development of novel approaches to treat the disease that might improve the response of patients who partially respond to the treatments focused on targeting mTORC1,” Sardiello said.

5 Simple Tinnitus Remedies to Relieve Ringing in the Ears

What is Tinnitus?

Before looking at tinnitus remedies to relieve ringing in the ears, it will be beneficial to get a good understanding of what tinnitus actually is, its symptoms, causes and mainstream treatment…

First off, tinnitus is not a disease or illness. You see, tinnitus — often referred to as ‘ringing in the ears’ — is a symptom of some other underlying problem. For example, one of the chief causes of tinnitus is noise-damaged hearing.

Tinnitus is just the perception of sounds that don’t have an external source. And the mild form of ringing in the ears is very common, with around 10% of people suffering mild tinnitus on occasion. But the number of people who get tinnitus so severely that it prevents them leading a normal life is as high as 1 in 200.

Tinnitus Symptoms

Tinnitus symptoms are the noises a sufferer hears in their head or ears. These sounds can be described as ringing, buzzing, roaring, swishing, whooshing, hissing, ticking, clicking, etc.

And they can be constant, intermittent, severe, mild, and so on, depending on each individual case. The kind of sound heard, e.g. hissing, clicking, etc., may be dependent on the underlying issue(s) causing the tinnitus.

Tinnitus Causes

As mentioned at the beginning, tinnitus is actually a symptom of some underlying issue or problem, not a disease or illness in itself. The underlying causes of tinnitus are many and varied and include:-

  • Hearing damaged by loud noise.
  • Age-related hearing loss.
  • Impacted earwax.
  • Ear infections / inflammations.
  • Head injury / whiplash.
  • Acoustic neuroma (benign tumour of the auditory nerve).
  • High blood pressure (hypertension).
  • Anemia.
  • Stress / anxiety / depression.
  • Atherosclerosis (narrowing of the arteries).
  • Middle ear effusion (sometimes called ‘glue ear’).
  • Twisted / kinked arteries in head / neck.
  • Glomus tumour (benign tumour commonly found in the middle ear).
  • Benign intracranial hypertension (increased pressure in the fluid around the brain).
  • Intracranial vascular lesions (abnormal artery – vein connections).
  • Venous hum (increased blood flow through jugular vein).
  • Otosclerosis (tiny bones in middle ear become stiff and less mobile).
  • Sinus allergies / inflammation.
  • Vitamin B12 deficiency.
  • Meniere’s disease (resulting from increased pressure in the inner ear).
  • Eustachian tube blockage (the tube equalizes middle ear / atmospheric pressure, and, drains mucous).
  • Lyme disease (disease acquired through tick bites).
  • Thyroid problems.
  • Some drug therapy such as aspirin, quinine, diuretics, chemotherapy, analgesics, antibiotics, etc.

Anatomy of the Human Ear

Subjective Tinnitus

Subjective tinnitus is the most common form of ringing ears by far. It is the name given to the type of tinnitus wherein it is only the victim who actually hears the sounds. No other person, including medical personnel using audio instruments, can hear them. Hence ‘subjective.’

But, be in no doubt, the sufferer does actually hear the sounds, they aren’t a figment of their imagination. And they can be so severe as to seriously disrupt their everyday lives.

One of the main causes is hearing loss, which can be brought about by issues like excessive noise, age-related hearing loss, impacted ear wax, Meniere’s disease, ear infection, middle ear effusion, acoustic neuroma, and some drugs such as aspirin, analgesics, diuretics, antibiotics, quinine, naproxen.

Other causes are head trauma, whiplash, thyroid problems, vitamin B12 deficiency, iron deficiency, depression, anxiety, etc.

Objective Tinnitus

Objective tinnitus is the condition where both the tinnitus sufferer and a medical professional can hear the sounds. The professional can hear them with the aid of an audio instrument as simple as a stethoscope.

Objective tinnitus is usually the result of some sort of arterial disturbance — turbulent blood flow — in the head and / or neck.

A particular type of ringing in the ears that falls into this category is ‘pulsatile tinnitus.’ This is so-called because the sounds that can be heard are rhythmic and can pulse in time with the patient’s heartbeat.

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4 Tips for Dressing Professionally with Psoriasis

I had been suffering with intermittent psoriasis for years and didn’t know what it was. Then I relocated from Atlanta to New York in 2011. The stress of moving brought out all the symptoms of my psoriasis and psoriatic arthritis (PsA) at once, making it easy to diagnose.

I was working at a prestigious law firm and new on the job. I had lesions on the tops of both of my feet and plantar psoriasis on the soles of my feet. Other areas were flaring, but I could easily cover them up with clothing.

I was terrified that other folks would see my lesions and didn’t even want to look at them myself. I had just bought new clothes to wear to work, including suits with skirts. If that wasn’t enough, my PsA was causing deformities in my feet, and my physician wanted me to wear sneakers!

Despite all of this, here’s how I got through it and kept my professional dignity.

1. Be honest about your condition

Openly talking about my condition was something I was very nervous about. After all, I was a new employee. Plus, I was a southern transplant, so I stuck out like a sore thumb already.

As it turned out, my human resources supervisor had lived with psoriasis since she was a teen! She really understood what I was going through. She assured me I could wear any footwear the doctor recommended, and she would field any questions about it on my behalf.

I’m not promising it will be this easy for you, but it’s always good to have someone in authority in your corner.

2. Consider wearing a lighter color palette for affected areas

Flakes are fun, aren’t they? If you deal with them on a regular basis, you may not have much navy blue or black in your closet.

Even though black tends to be a staple color in New York, there were times I had to go with a medium gray in the autumn and winter. This helped minimize the appearance of flakes on my clothes.

Sometimes your scalp may be the only affected area. Lighter dress shirts for men or blouses for ladies will help greatly.

3. Colored opaque tights can mask spots and red patches

I wore a lot of skirt suits and even dresses in the spring and summer. Colored tights became my best friends! I bought them in every shade. They made me look more put together and my lesions didn’t show through when I paired them with loafers or flats.

4. Forget heels and dress shoes if you have plantar psoriasis

Men, feel free to keep your footwear, so long as it’s still comfortable for you. Ladies, I know you don’t want to hear this, but binding shoes and high heels may be making your plantar psoriasis worse. Skin irritation encourages plaques.

If you can’t get permission to wear sneakers during a flare, consider keeping a pair of cozy slippers under your desk to wear while you are seated.

The takeaway

While psoriasis can make dressing for a professional setting slightly more difficult, it doesn’t have to be. Be open with your supervisors, and find what works best for you to remain comfortable and confident.

9 Things I Have Learned From Living With Ulcerative Colitis

It has been almost 12 years since I was diagnosed with ulcerative colitis and I have learned a lot since then. As a sixth grader, I had no idea what my diagnosis would mean, but it has most certainly changed my life. Before getting into what I have learned, here’s a brief synopsis of my story.

I was originally told by a doctor who I met only once that I did not have enough fiber in my diet. Anyone want to take a guess how that went when I began to increase my fiber intake? You guessed it. The symptoms got 10 times worse. After that disaster, another doctor had me get an endoscopy, a barium x-ray and a colonoscopy. From that experience, I discovered I never want to get a barium x-ray again. When that was all said and done, I was diagnosed with ulcerative colitis. Since then, I have found out that my case is a little more along the lines of the Crohn’s disease, but it does not change the medication I need to take. From the regular colonoscopies to the bad days, I have learned what it means for me to have ulcerative colitis (UC). While no one has the same experience, this is what I have learned over the years about my UC. I still have plenty to learn, but these are some of the things I have learned that have changed my life.

1. You will continue finding out that people you have known for years have a similar diagnosis.

This never ceases to amaze me. Over the years, I have discovered that so many people I know have UC, Crohn’s or some form of inflammatory bowel disease (IBD). Not surprisingly, it makes you feel way more comfortable with that person. It’s like a bonding experience. If I have a question to ask them about their experiences, I know they are always open to talk about it. Bathroom talk is widely accepted in the IBD community, and I very much appreciate that. If we’re being honest, you really can’t be diagnosed with any form of IBD and not appreciate poop jokes.

2. You will never stop learning about your condition.

And no one wants to hear about the gross details…what a bummer. Pun intended.

3. You will have really terrible days, and you won’t be able to do anything about it.

I have figured out that laying on my stomach sometimes relieves pain, but on many of my worst days, I can’t even stand up straight. Other than that, I can only crawl around the house while staying close to the bathroom. No matter what anyone says, staying at home on bad days is actually not even close to being great. I feel completely helpless and basically all I can think about is how much pain I am in and how ridiculously unproductive I am being.

4. You will figure out who understands invisible diseases.

From family members to teachers, some people just don’t get it. I’ve been so blessed with amazing people in my life that are understanding, but it’s surprising who doesn’t believe you. “You don’t look sick, though…” Thank you…?

5. Colonoscopies are actually awesome.

ab7603b82a29882e53468b022fe6b88eSome may disagree, but stepping on the scale after a clean-out is pretty cool. I also really dig the deep sleep and the cool socks you get to wear during the procedure. During the first colonoscopy I had as a pediatric patient, I was given a stuffed animal. I told my mom it was like we bought the stuffed animal and I got a free colonoscopy with it. She informed me that would probably not be a big selling point. Weird.

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Ankylosing Spondylitis: 9 Ways To Reduce Inflammation

If you’re experiencing ankylosing spondylitis symptoms like joint pain, stiffness, and swelling, taking these steps to reduce inflammation in your body may help.

When you have ankylosing spondylitis — as with any other form of arthritis — your condition may be sensitive to the overall level of inflammation in your body. Inflammation is a body-wide response designed to help fight infections and heal injuries, and in these situations, it can be crucial to your well-being.

But when you have a condition like ankylosing spondylitis, inflammation can increase symptoms of pain, stiffness, and swelling. “Any time you have an autoimmune condition, when there’s inflammation in the body, you’re more susceptible to flares,” says Gerardo Miranda-Comas, MD, a rehabilitation and physical medicine specialist at Mount Sinai Medical Center in New York City.

Inflammation can also cause more lasting damage. “In diseases like ankylosing spondylitis, long-term inflammation can lead to bony damage and fusion of joints,” says Kevin Deane, MD, a rheumatologist at University of Colorado Hospital in Aurora. “And that can lead to lack of motion and really disabling arthritis down the road.”

The good news is that there are several steps you can take to minimize inflammation in your body. Try these tips to reduce inflammation and improve the outlook of anykylosing spondylitis.

1. Take your medications as directed.

Drugs used to treat ankylosing spondylitis — whether they’re over-the-counter non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen, or prescription therapies like TNF inhibitors — all have the effect of reducing chronic inflammation in the body.

People with ankylosing spondylitis should consider “following what their healthcare providers and rheumatologists recommend” in terms of drug therapies to be a key step in reducing inflammation, says Deane.

2. If you smoke tobacco, quit.

According to Deane, not smoking is probably the single most important lifestyle factor to reduce inflammation in ankylosing spondylitis. If you smoke, he says, quitting is “critically important.”

“We know that smoking drives the immune system, revs it up, and makes inflammation worse,” he says.

There’s a large body of evidence that links smoking to increased inflammation in the body. One recent example, published in March 2017 in the journal BMC Complementary and Alternative Medicine, showed that smokers had higher levels of high sensitive C-reactive protein — a marker of inflammation — than nonsmokers.

3. Include good fats in your diet.

While there isn’t any perfect, proven diet for ankylosing spondylitis, Deane says that following a Mediterranean-type diet — rich in fruits and vegetables, whole grains, olive oil, nuts and seeds, and fish — is probably the best way of eating to reduce inflammation in the body.

Omega-3 fatty acids, in particular — found in certain fatty fish, nuts, and seeds — may help counter inflammation. In a study published in March 2017 in the Scandinavian Journal of Rheumatology, researchers found that people with psoriatic arthritis — an inflammatory type of arthritis closely related to ankylosing spondylitis — who took omega-3 supplementsexperienced less disease activity, showed lower markers of inflammation, and required lower doses of medications to control their condition.

On the other hand, Miranda-Comas notes, saturated fats like those found in red meat and full-fat dairy have been linked to pro-inflammatory processes in the body and should be avoided as much as possible.

4. Avoid high-heat cooking.

According to the Arthritis Foundation, cooking food at high temperatures can lead to the formation of chemicals called advanced glycation end products (AGEs), which can trigger your body’s inflammatory response and have been linked to a number of different health conditions.

To reduce AGEs in your diet, it’s especially important not to use high heat to grill, sear, or fry beef, pork, chicken, and fish.

5. Try using anti-inflammatory spices.

Incorporating spices like garlic, turmeric, ginger, cinnamon, and cayenne pepper into your diet may help reduce inflammation, according to the Arthritis Foundation.

Deane notes that when people make efforts to include these spices in their diet, “They often change their cooking habits to incorporate these potentially very valuable items” — increasing their intake of vegetables and reducing fried foods in the process, which helps reduce inflammation even further.

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